Sweet’s Syndrome, Photosensitivity & Photoexacerbated Dermatoses.

Updated 6/02/17.

What is photosensitivity?

Photosensitivity is a sensitivity to sunlight or ultraviolet (UV) light, and can sometimes increase your risk of sunburn, depending upon the cause. In some people, photosensitivity can cause a skin rash or other type of skin lesion, and skin lesions triggered by sunlight or UV light are called photodermatoses.

What are photoexacerbated dermatoses?

Photoexacerbated dermatoses are a form of photodermatoses caused by a pre-existing condition or skin disease. They can get worse on exposure to sunlight or UV light. Photoexacerbated dermatoses include:

  • Lupus erythematosus (Oakley, 2016).
  • Dermatomyositis.
  • Darier disease.
  • Rosacea.
  • Pemphigus vulgaris.
  • Pemphigus foliaceus.
  • Atopic dermatitis.
  • Psoriasis (Ibid).

Is Sweet’s syndrome a type of photoexacerbated dermatosis?


In 2011, Sweet’s syndrome was experimentally induced in a 78-year-old man by exposing him to UV light, and in 2014, Sweet’s syndrome lesions developed on the arms and back of a 40-year-old woman who had been working in the sun (Meyer et al, 2011; Verma et al, 2014).

Why does this happen?

As yet, it is not fully understood why sunlight or UV light can sometimes trigger Sweet’s syndrome, and a lot more research is required. However, there are two theories as to why this might happen.


Koebner phenomenon or isomorphic response (Meyer et al, 2011; Verma et al, 2014).

What does this mean?

This means that in areas where the skin is damaged or irritated by overexposure to sunlight or UV light, skin lesions could develop.

Please note that patients with Sweet’s syndrome can also demonstrate a very similar kind of response to Koebner phenomenon or isomorphic response. This is referred to as pathergy. Read more here.


Overexposure to UV-B light (shortwave light that causes skin reddening and sunburn) leading to the activation of white blood cells called neutrophils as a result of cytokine production (Meyer et al, 2011; Verma et al, 2014).

What does this mean?

This means that when the cells of the skin are damaged by sun, cells next to the damaged cells start spreading cytokines. These are proteins and molecular messengers that are stored by the cells of the immune system. When these cytokines are released, this causes inflammation as the first response of the immune system to destroy the damaged cells after which the damaged skin starts to heal. Certain cytokines have been proven to play a role in Sweet’s syndrome, including endogenous granulocyte colony-stimulating factor (G-CSF), which can promote the production of neutrophils. Patients with active Sweet’s syndrome usually have an increased number of neutrophils in their blood, and neutrophils also infiltrate their tissues, particularly the skin. Read more here.

Important information!

Dapsone and tetracycline antibiotics, e.g. minocycline and doxycycline, are treatments for Sweet’s syndrome. They are known to cause photosensitivity, and this can increase the risk of sunburn.


Oakley, A. (2016) Photosensitivity. DermNet NZ (online). Originally published in 1997. Updated by Professor Oakley, Jan 2016.

Meyer, V., Schneider, S., Bonsmann, G. and Beissert, S (2011) Experimentally Confirmed Induction of Sweet’s Syndrome by Phototesting.  ACTADERMATO-VENEREOLOGICA (online).

Verma, R., Vasudevan, B. and Mitra, D. (2014) Unusual presentation of idiopathic sweet’s syndrome in a photodistributed pattern. Indian Journal of Dermatology; 59(2): 186-189 (online).

Other information.

Ngan, V. (2006) Drug-induced photosensitivity. DermNet NZ (online). Accessed 06/02/17.

© 2012-2017 Sweet’s Syndrome UK


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